title: Diesel exhaust inhalation increases thrombus formation in man.
abstract: OBJECTIVE
  Although the mechanism is unclear, exposure to traffic-derived air pollution is a trigger for acute myocardial infarction (MI). The aim of this study is to investigate the effect of diesel exhaust inhalation on platelet activation and thrombus formation in men.
  
  
  RESULTS
  In a double-blind randomized crossover study, 20 healthy volunteers were exposed to dilute diesel exhaust (350 microg/m(3)) and filtered air. Thrombus formation, coagulation, platelet activation, and inflammatory markers were measured at 2 and 6 h following exposure. Thrombus formation was measured using the Badimon ex vivo perfusion chamber. Platelet activation was assessed by flow cytometry. Compared with filtered air, diesel exhaust inhalation increased thrombus formation under low- and high-shear conditions by 24% [change in thrombus area 2229 microm(2), 95% confidence interval (CI) 1143-3315 microm(2), P = 0.0002] and 19% (change in thrombus area 2451 microm(2), 95% CI 1190-3712 microm(2), P = 0.0005), respectively. This increased thrombogenicity was seen at 2 and 6 h, using two different diesel engines and fuels. Diesel exhaust also increased platelet-neutrophil and platelet-monocyte aggregates by 52% (absolute change 6%, 95% CI 2-10%, P = 0.01) and 30% (absolute change 3%, 95% CI 0.2-7%, P = 0.03), respectively, at 2 h following exposure compared with filtered air.
  
  
  CONCLUSIONS
  Inhalation of diesel exhaust increases ex vivo thrombus formation and causes in vivo platelet activation in man. These findings provide a potential mechanism linking exposure to combustion-derived air pollution with the triggering of acute MI.
authors.affiliation: Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK. andrew.lucking@btinternet.com
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Lucking
authors.forename: Magnus
authors.initials: M
authors.lastname: Lundback
authors.forename: Nicholas L
authors.initials: NL
authors.lastname: Mills
authors.forename: Dana
authors.initials: D
authors.lastname: Faratian
authors.forename: Stefan L
authors.initials: SL
authors.lastname: Barath
authors.forename: Jamshid
authors.initials: J
authors.lastname: Pourazar
authors.forename: Flemming R
authors.initials: FR
authors.lastname: Cassee
authors.forename: Kenneth
authors.initials: K
authors.lastname: Donaldson
authors.forename: Nicholas A
authors.initials: NA
authors.lastname: Boon
authors.forename: Juan J
authors.initials: JJ
authors.lastname: Badimon
authors.forename: Thomas
authors.initials: T
authors.lastname: Sandstrom
authors.forename: Anders
authors.initials: A
authors.lastname: Blomberg
authors.forename: David E
authors.initials: DE
authors.lastname: Newby
mesh_terms: D000328:Adult; D035843:Biomedical Research; D002985:Clinical Protocols; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004781:Environmental Exposure / Q000009:adverse effects* / Q000517:prevention & control; D005434:Flow Cytometry / Q000379:methods; D006801:Humans; D019570:Inhalation Exposure / Q000517:prevention & control; D008297:Male; D052638:Particulate Matter; D015539:Platelet Activation; D018570:Risk Assessment; D013927:Thrombosis / Q000209:etiology* / Q000378:metabolism; D001335:Vehicle Emissions / Q000633:toxicity*; D055815:Young Adult
chemical_list: D052638:Particulate Matter; D001335:Vehicle Emissions